title: Octreotide lessens peritoneal injury in experimental encapsulated peritoneal sclerosis model.
abstract: OBJECTIVE
  Encapsulated peritoneal sclerosis is characterized by neoangiogenesis and fibrosis. Octreotide, a somatostatin analogue is a well-known antifibrotic, antiproliferative and anti-angiogenic agent. The aim of the study is to evaluate the effects of octreotide in encapsulated peritoneal sclerosis-induced neoangiogenesis and fibrosis and compare the results with resting.
  
  
  METHODS
  Non-uraemic Wistar-Albino male rats (n = 35) were divided into four groups. Group I, control rats, received 2 mL isotonic saline i.p. daily for 3 weeks. Group II, received daily i.p. 2 mL/200 g injection of chlorhexidine gluconate (0.1%) and ethanol (%15) dissolved in saline for 3 weeks. Group III, chlorhexidine gluconate for 3 weeks plus an additional 3 weeks without any treatment (rest), to a total of 6 weeks. Group IV, chlorhexidine gluconate for 3 weeks plus an additional 3 weeks octreotide, 50 mcg/kg bodyweight s.c., for a total of 6 weeks.
  
  
  RESULTS
  Octreotide significantly reversed ultrafiltration capacity of peritoneum with decreasing inflammation, neoangiogenesis and fibrosis compared to the resting group. Octreotide also caused inhibition of dialysate transforming growth factor-β1, vascular endothelial growth factor and monocyte chemotactic protein-1 activity and improved mesothelial cell cytokeratin expression. Peritoneal resting has no beneficial effects on peritoneum.
  
  
  CONCLUSIONS
  In conclusion, octreotide may have a therapeutic value in peritoneal dialysis patients who suffer from encapsulated peritoneal sclerosis.
authors.affiliation: Nephrology Department, Ege University, Izmir, Turkey.
authors.forename: Muhittin
authors.initials: M
authors.lastname: Ertilav
authors.forename: Ender
authors.initials: E
authors.lastname: Hur
authors.forename: Devrim
authors.initials: D
authors.lastname: Bozkurt
authors.forename: Savas
authors.initials: S
authors.lastname: Sipahi
authors.forename: Ozge
authors.initials: O
authors.lastname: Timur
authors.forename: Banu
authors.initials: B
authors.lastname: Sarsik
authors.forename: Fehmi
authors.initials: F
authors.lastname: Akcicek
authors.forename: Soner
authors.initials: S
authors.lastname: Duman
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D018932:Chemokine CCL2 / Q000378:metabolism; D002710:Chlorhexidine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000378:metabolism; D015314:Dialysis Solutions / Q000008:administration & dosage / Q000378:metabolism; D004195:Disease Models, Animal; D005355:Fibrosis; D008297:Male; D009389:Neovascularization, Pathologic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015282:Octreotide / Q000494:pharmacology*; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D056627:Peritoneal Fibrosis / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D010537:Peritoneum / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010539:Permeability; D051381:Rats; D017208:Rats, Wistar; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D000893:Anti-Inflammatory Agents; C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D015314:Dialysis Solutions; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; C010882:chlorhexidine gluconate; D002710:Chlorhexidine; D015282:Octreotide